The burn patient has a greatly increased risk of developing bacterial septicemia because he has undergone adverse alterations in both his specific immune and nonspecific inflammatory host resistance systems. We have attempted to identify inimical alterations in those regulatory interactions which control immunocompetence. Assays are described which monitor postburn changes in the following functions: Monocyte production of Plasminogen Activator (PA), generation of tissue procoagulant factor (TF), and synthesis of prostaglandin E2 (PGE2). We have correlated the patients' altered M phi functions to aberrations in mitogen responses, an increase in suppressor T cell activity, or an increase in inhibitory M phi functions. Significant alterations in M phi and immune cell interactions were seen in thermally injured patients. All of the thermally injured patients identified as having decreased immune responses experience major septic complications. The data from this project are indicative of some of the burn mediated mechanisms involved in depressed immunocompetance after thermal injury. Discernment of the underlying mechanisms which cause loss of host resistance will facilitate development of therapy designed to prevent or attenuate the adverse post-burn changes in the immune system.